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巨细胞PTP1B通过JAK2/STAT3-OPA1轴调节线粒体动力学,并激活cGAS/STING信号通路

Xuefeng Lei¹, Diandian Qian², Wenzheng Zhang¹

¹Department of Orthopaedics, Yangpu Hospital, School of Medicine, Tongji University, Shanghai, China.

Frontiers in immunology

|October 24, 2025

概括

巨细胞蛋白氨酸酸酶1B (PTP1B) 通过破坏线粒体功能和通过JAK2/STAT3-OPA1和cGAS/STING通路促进炎症来驱动肌病. 准PTP1B为肌损伤提供了一个潜在的治疗策略.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

肌病包括肌退化,巨细胞驱动的炎症和线粒体功能障碍.
蛋白氨酸酸酶1B (PTP1B) 在肌病期间在巨细胞中被上调.
在肌病的条件下,JAK2/STAT3信号通路通常被抑制.

研究的目的:

为了研究巨细胞PTP1B在肌病变的发病过程中的作用.
阐明将PTP1B与肌中的炎症和线粒体功能障碍联系起来的分子机制.
探索PTP1B作为肌病的潜在治疗标.

主要方法:

肌病组织的生物信息学分析.
使用带有条件巨细胞特异性PTP1B删除 (Ptpn1-/-) 的肌病小鼠模型.
在体内实验中评估信号通路 (JAK2/STAT3,cGAS/STING) 和线粒体动力学 (OPA1,mtDNA释放).

主要成果:

巨细胞PTP1B的上调与肌病中的免疫激活和JAK2/STAT3抑制相关.
条件删除巨细胞PTP1B可以缓解肌炎症和纤维化.
PTP1B抑制STAT3激活,抑制OPA1,导致线粒体分裂,mtDNA释放,并激活cGAS/STING通路,增加炎症.

结论:

巨细胞PTP1B是肌病的关键媒介,通过JAK2/STAT3-OPA1轴调节线粒体动态.
通过激活cGAS/STING炎症通路,PTP1B会加剧肌损伤.
向PTP1B为治疗肌病症提供了一个有前途的治疗途径.

关键词:

通过JAK2/STAT3信号通道传输信号.这就是PTP1B.巨细胞是什么?巨细胞是什么?线粒体的动力学肌病变是一种肌病变.

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